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Critical Reviews™ in Biomedical Engineering
SJR: 0.207 SNIP: 0.376 CiteScore™: 0.79

ISSN Imprimir: 0278-940X
ISSN En Línea: 1943-619X

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Critical Reviews™ in Biomedical Engineering

DOI: 10.1615/CritRevBiomedEng.v29.i2.20
pages 247-278

Mechanics of Endothelial Cell Architecture and Vascular Permeability

Ann L. Baldwin
Department of Physiology, College of Medicine, University of Arizona, Tucson, AZ 85724-5051
Gavin Thurston
Department of Anatomy, 3rd and Parnassus, University of California, San Francisco, CA 94143-0452


Blood vessel walls form a selective barrier to the transport of materials between blood and tissue, and the endothelium contributes significantly to this barrier function. The role of the endothelium is particularly important in thin-walled vessels, such as venules, because during tissue inflammation the endothelial junctions widen in localized areas and gaps form, thus compromising the barrier function. The mechanisms of endothelial gap formation are still under question. In this review we describe what is known about the structure of endothelial cell-cell junctions and how this structure can change during inflammation. We then consider two possible mechanisms by which endothelial gaps are formed: active endothelial cell contraction or breakdown of the junctional complex, followed by passive recoil. Using measured values of the mechanical properties of endothelial cells, and the forces to which they are subjected, we calculate that gap formation by breakdown of cellular adhesion, followed by passive recoil, is a feasible mechanism. Finally, since endothelial cell surfaces, including junctions, are coated with a glycocalyx, we consider the question of whether changes in the glycocalyx can markedly increase endothelial permeability. We conclude that gap formation can occur by active contraction or by breakdown of adhesion, depending on the inflammatory mediator, and that the responses of the glycocalyx may also play an important role in the regulation of microvascular permeability.

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